Using 50 mongrel dogs with alveolar flooding produced by oleic acid administration, the possible roles of vasoactive cyclooxygenase products on intrapulmonary shunt flow (Q̇(S)/Q̇(T)) and extravascular lung water (ETVI) in acutely injured lungs were assessed. Suppressing cyclooxygenase activity with indomethacin administration diminished the concentrations of thromboxane (TX) B2 and 6-keto-prostaglandin F(1α) (6-keto-PGF(1α)) in arterial blood, resulting in a significant refuction in Q̇(S)/Q̇(T). Furthermore, indomethacin completely suppressed the increase in ETVI. Inhibition of TXA2 generation by OKY-046 (thromboxane A2 synthase blocker) diminished the concentration of TXB2 while increasing that of 6-keto-PGF(1α) in blood. Administration of either OKY-046 or synthetic prostacyclin (PGI2) markedly enhanced Q̇(S)/Q̇(T), in association with an increase in ETVI. In conclusion, the potent vasodilator prostacyclin was considered to enhance shunt flow, leading to the augmentation of edema formation.
|ジャーナル||Japanese Journal of Thoracic Diseases|
|出版ステータス||Published - 1994 1月 1|
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